T regulatory cells (Tregs) are important cells required for modulation of the immune system, maintaining tolerance to self-antigens and suppression of autoimmune diseases. The emergence of Tregs as a significant component of immune homeostasis provides a potential therapeutic opportunity for active immune regulation and long-term tolerance induction. Indeed, deficiency of naturally occurring T-regulatory cells (nTregs) has been observed in a variety of autoimmune conditions (36, 37). Moreover, adoptive transfer of polyclonal or antigen selected nTregs has been found to overcome autoimmune and allergic conditions (38-40). However, a limitation that prevents therapeutic utilization of Tregs in autoimmune diseases is the relative difficulty in obtaining large numbers of Tregs. Although much is known about T-cell receptor (TCR) mediated T cell activation and proliferation (25), signaling required for Treg proliferation in the absence of TCR stimulation remains largely unknown. Thus, an effective method for expanding Tregs is still needed.